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MiR-26a inhibits proliferation and migration of breast cancer through repression of MCL-1.

Gao J, Li L, Wu M, Liu M, Xie X, Guo J, Tang H, Xie X - PLoS ONE (2013)

Bottom Line: MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression.MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines.Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Oncology, Sun Yat-sen University Cancer Center, Guangzhou, PR China.

ABSTRACT
Breast cancer is the most commonly malignancies in women. MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression. MiR-26a has been reported as a tumor suppressor microRNA in breast cancer, which is attributed mainly to targeting of MTDH and EZH2, however, the expression profile and therapeutic potential of miR-26a is still unclear. Here we demonstrate that miR-26a is down-regulated in breast cancer cells and clinical specimens and its modulation in breast cancer cells regulates cell proliferation, colony formation, migration and apoptosis. MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines. It was further explored that miR-26a increased sensitivity of breast cancer cells to paclitaxel in which MCL-1 was involved. Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

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MiR-26a sensitized breast cancer cells to paclitaxel.A. Viability of MDA-MB-231, MCF-7, MDA-MB-435, MDA-MB-468 cells was determined by MTT assay 72 hours after treatment. The percentage of the cell viability as compared with itself without paclitaxel treatment was presented. The concentrations of miR-26a and paclitaxel were 50 µM and 0.12 nM, respectively. B. Western blot assay for MCL-1 expression 48 hours after treatment in MDA-MB-231 cells. *P<0.05.
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pone-0065138-g007: MiR-26a sensitized breast cancer cells to paclitaxel.A. Viability of MDA-MB-231, MCF-7, MDA-MB-435, MDA-MB-468 cells was determined by MTT assay 72 hours after treatment. The percentage of the cell viability as compared with itself without paclitaxel treatment was presented. The concentrations of miR-26a and paclitaxel were 50 µM and 0.12 nM, respectively. B. Western blot assay for MCL-1 expression 48 hours after treatment in MDA-MB-231 cells. *P<0.05.

Mentions: Given that paclitaxel was involved in the majority of strategies of conventional chemotherapy, and several miRNAs have been reported to have the synergistic anti-tumor effects with conventional chemotherapy [26], the raised question was whether miR-26a could enhance the therapeutic effect of paclitaxel in breast cancer cells. In order to find the answer, MTT assay was performed 72 hours after the treatment of miR-26a and paclitaxel. As shown in Fig. 7A, the combination treatment caused greater inhibition of cell growth, as compared with paclitaxel alone. This result suggested that miR-26a effectively sensitized breast cancer cells to paclitaxel.


MiR-26a inhibits proliferation and migration of breast cancer through repression of MCL-1.

Gao J, Li L, Wu M, Liu M, Xie X, Guo J, Tang H, Xie X - PLoS ONE (2013)

MiR-26a sensitized breast cancer cells to paclitaxel.A. Viability of MDA-MB-231, MCF-7, MDA-MB-435, MDA-MB-468 cells was determined by MTT assay 72 hours after treatment. The percentage of the cell viability as compared with itself without paclitaxel treatment was presented. The concentrations of miR-26a and paclitaxel were 50 µM and 0.12 nM, respectively. B. Western blot assay for MCL-1 expression 48 hours after treatment in MDA-MB-231 cells. *P<0.05.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3672200&req=5

pone-0065138-g007: MiR-26a sensitized breast cancer cells to paclitaxel.A. Viability of MDA-MB-231, MCF-7, MDA-MB-435, MDA-MB-468 cells was determined by MTT assay 72 hours after treatment. The percentage of the cell viability as compared with itself without paclitaxel treatment was presented. The concentrations of miR-26a and paclitaxel were 50 µM and 0.12 nM, respectively. B. Western blot assay for MCL-1 expression 48 hours after treatment in MDA-MB-231 cells. *P<0.05.
Mentions: Given that paclitaxel was involved in the majority of strategies of conventional chemotherapy, and several miRNAs have been reported to have the synergistic anti-tumor effects with conventional chemotherapy [26], the raised question was whether miR-26a could enhance the therapeutic effect of paclitaxel in breast cancer cells. In order to find the answer, MTT assay was performed 72 hours after the treatment of miR-26a and paclitaxel. As shown in Fig. 7A, the combination treatment caused greater inhibition of cell growth, as compared with paclitaxel alone. This result suggested that miR-26a effectively sensitized breast cancer cells to paclitaxel.

Bottom Line: MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression.MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines.Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Oncology, Sun Yat-sen University Cancer Center, Guangzhou, PR China.

ABSTRACT
Breast cancer is the most commonly malignancies in women. MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression. MiR-26a has been reported as a tumor suppressor microRNA in breast cancer, which is attributed mainly to targeting of MTDH and EZH2, however, the expression profile and therapeutic potential of miR-26a is still unclear. Here we demonstrate that miR-26a is down-regulated in breast cancer cells and clinical specimens and its modulation in breast cancer cells regulates cell proliferation, colony formation, migration and apoptosis. MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines. It was further explored that miR-26a increased sensitivity of breast cancer cells to paclitaxel in which MCL-1 was involved. Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

Show MeSH
Related in: MedlinePlus